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A Pipeline to Investigate the Structures and Signaling Pathways of Sphingosine 1-Phosphate Receptors
Published on: June 8, 2022
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Sphingosine-1-phosphate expression in human epiretinal membranes.
Minho Kim1, Soonil Kwon2, Sohee Jeon3
1Apgujung St. Mary's Eye Center, Seoul, Republic of Korea.
Plos One
|August 31, 2022
Summary
Abnormal posterior vitreous detachment (PVD) may cause epiretinal membrane (ERM) via Sphingosine-1-phosphate (S1P). S1P expression was found in ERM, and it increased Muller glial cell migration, suggesting its role in ERM development.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Abnormal posterior vitreous detachment (PVD) is implicated in epiretinal membrane (ERM) formation.
- The precise molecular mechanisms underlying ERM pathogenesis during PVD remain unclear.
- Sphingosine-1-phosphate (S1P) is a known mediator of mechanosensitive responses and may play a role in ERM development.
Purpose of the Study:
- To investigate the expression of S1P in human ERM specimens.
- To elucidate the role of S1P in the behavior of cultured human Muller glial cells.
Main Methods:
- Analysis of S1P expression in 24 human ERM specimens.
- Quantification of S1P+ cell density in relation to secondary ERM and ellipsoid zone (EZ) defects.
- In vitro experiments assessing the effect of S1P on human Muller glial cell migration, N-cadherin, and α-SMA expression.
Main Results:
- S1P expression was detected in 29.2% of ERM specimens.
- Significantly higher S1P+ cell density was observed in patients with secondary ERM (p=0.002) and EZ defects (p=0.036), indicative of abnormal PVD.
- S1P treatment enhanced Muller glial cell migration and increased N-cadherin and α-SMA expression.
Conclusions:
- S1P is present in human ERM and its expression correlates with indicators of abnormal PVD.
- S1P promotes Muller glial cell migration and expression of key proteins involved in cell adhesion and contractility.
- S1P is identified as a potential causative molecule in the development of ERM associated with abnormal PVD.

